Muscle contraction is a complicated series of reactions that begins with a nerve impulse also known as an action potential. An impulse travels from the brain and spinal cord to a motor neuron that interacts with the sarcolemma (plasma membrane) of a muscle fiber. Located at the end of the motor neuron is the axon terminal and the point at which it meets the muscle fiber is called the neuromuscular junction. Within the axon terminal, synaptic vesicles contain the necessary materials to ignite a reaction from the muscle fiber. Synaptic vesicles are membrane bound sacs which contain the neurotransmitter acetylcholine (ACh). Dividing the axon terminal and the sarcolemma is the synaptic cleft which provides a transitional path for acetylcholine to the muscle fiber. When the action potential reaches the axon terminal ACh is released into the synaptic cleft. At the surface of the sarcolemma are folded junctions called the motor end plate which receives ACh at receptor sites. Once ACh binds to the receptor site it triggers the opening of chemically gated ion channels which allows the passage of sodium ions into the muscle fiber. The entrance of sodium ions results in the action potential sweeping over the sarcolemma of the whole muscle. Depolarization of the sarcolemma occurs and travels along invaginations deep within the muscle fiber called t-tubules. Once voltage sensitive proteins among the t-tubules are stimulated by the current of the action potential it opens calcium ion channels located adjacent to the proteins. Open calcium channels release ions into the cytosol from storage sites of the muscle fiber, the sarcoplasmic reticulum (SR).
The presence of calcium is necessary to initiate movement of the contractile unit, or sarcomere, of each myofibril within a muscle fiber. Myosin and actin filaments responsible for contraction cannot interact without calcium because a blocking agent called tropomyosin prevents interaction. At the end of each tropomyosin rod is a complex called troponin, which binds to calcium as it enters the cell. When calcium and troponin join, troponin changes shape which causes tropomyosin to be released, leaving the binding myosin binding site available. The thick myosin heads are now able to attach and crawl along the thin actin filaments, drawing them towards the center of the sarcomere, this is the contractile movement of the fiber. The attraction of myosin heads to actin is referred to as a cross bridge formation. When the action potential ends calcium ions are returned to the SR via active transport, tropomyosin’s blocking characteristic is reestablished, disabling myosin binding sites and the muscle fiber returns to a relaxed state.
If a blocking agent such as metubine were present at the neuromuscular junction it would prevent acetylcholine from binding to receptor sites. Metubine, would act much like an enzyme inhibitor and compete for the binding site upon the motor end plate of the muscle fiber. If ACh is unable to bind and open the gated ion channel sodium will not be released and the depolarization of the rest of membrane will not occur. Without the wave of action potential contraction cannot take place.
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